CONTRATADOS
GIRARDI Elena Silvia
artículos
Título:
Modification of [3H]MK801 Binding to Rat Brain NMDA......
Autor/es:
GIRALDEZ L, GIRARDI E
Revista:
NEUROCHEMICAL RESEARCH
Editorial:
SPRINGER/PLENUM PUBLISHERS
Referencias:
Año: 1998 vol. 23 p. 1327 - 1327
ISSN:
0364-3190
Resumen:
Specific [3H]MK801 binding to rat brain NMDA receptors after the administration of the convulsant drug 3-mercaptopropionic acid (MP) and the adenosine analogue cyclopentyladenosine (CPA) was studied by means of a quantitative autoradiographic method. MP administration (150 mg/kg, i.p.) caused significant decreases in [3H]MK801 binding in several hippocampus subareas and layers, mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [3H]MK801 binding in several layers of CA1 and CA3 of hippocampus (11-27%) and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [3H]MK801 binding in several layers of CA1 and CA3 of hippocampus (11-27%) and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [3H]MK801 binding in several layers of CA1 and CA3 of hippocampus (11-27%) and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [3H]MK801 binding in several layers of CA1 and CA3 of hippocampus (11-27%) and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [3H]MK801 binding in several layers of CA1 and CA3 of hippocampus (11-27%) and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. drug 3-mercaptopropionic acid (MP) and the adenosine analogue cyclopentyladenosine (CPA) was studied by means of a quantitative autoradiographic method. MP administration (150 mg/kg, i.p.) caused significant decreases in [3H]MK801 binding in several hippocampus subareas and layers, mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [3H]MK801 binding in several layers of CA1 and CA3 of hippocampus (11-27%) and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [3H]MK801 binding in several layers of CA1 and CA3 of hippocampus (11-27%) and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [3H]MK801 binding in several layers of CA1 and CA3 of hippocampus (11-27%) and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. and in CA1, CA2, CA3 (24-35%) after CPA+MP postseizure, and an increase in CA2 after CPA and CPA+MP postseizure (20-34%), were observed. A drop was found in the occipital subarea (18-24%) after CPA and in the frontal and occipital subarea after CPA+MP postseizure (24-34%) while no changes were observed in any treatment involving the other cerebral cortex regions, thalamic nuclei, caudate putamen and olfactory tubercle. These results show that [3H]MK801 binding changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. changes according to drug treatment and the area being studied, thus indicating a different role in seizure activity. mainly in CA1 and CA3 at seizure (11-27%) and postseizure (8-16%) and in cerebral occipital cortex at seizure (18-22%). In nucleus accumbens, a rise was observed at postseizure (44%) and a tendency to increase at seizure (24%). CPA (2mg/kg, i.p.) decreased ligand binding in hippocampus (CA1, CA2, CA3) (17-22%) and in occipital cerebral cortex (18-24%). When CPA was administered 30 minutes before MP (which delayed seizure onset) and rats were sacrified at seizure, decreases in [
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